neuro Flashcards
(280 cards)
1
Q
patients with parkinsons can also have what
A
POTS- even more increased risk of fall on top of the shuffle gait, bradykinesia
2
Q
whats symtpoms of psychosis
A
delusions
hallucinations
like short term schitzopherenia
not looking after self, pull away from family
3
Q
what can cause psychosis
A
drug induced
stress
long use of corticosteroids
can go but can remain
4
Q
whatsthe two types of stroke
A
ischemia/ infarction
intracranial haemorrahgic
5
Q
what can cause a disruption of blood supply to the brain
A
thrombus formation/ embolus
athelerosclerosis
shock
vasculitis
6
Q
whats a tia
A
transient ischemic attack
symtpoms resolve wothing 24 hrs- no lasting issues
new defiition = transient neurological dysfunction secondary to ischemia without infarction
7
Q
what does having a tia mean and what score do you use
A
means often preced a full stroke
crescendo tia = have 2 or more tia within 1 week increase progression to stroke
use the ABCD2 score to see the risk of the having a storke within 48 hrs
rosier score to see how likely going to have a stroke = above 0 is stroke likely
8
Q
whats the causes/ risk factors of stroke/TIA
A
hypertension
AF
cv disease- mi, angina, peripheral vascualr disease
carotid artery disease
diabetes
smoking
vasculitis
thrombophila
COCP
blood disorders
cerebal anyersm
brain tumour
atherloscleoris
ADPKD- formaition of anyrsm more liekly
small vessel disease
9
Q
what can cause disru[tion to nlood supply
A
thrombus/ embolism
shock
vasculitis
athelrosclerosis
10
Q
whats the presentation of a stroke
A
sudden onset!
sudden…
typically asymmetrical
weakness of limbs
facial weakness
speech - dysphasia
visual/sensory loss
thundeclap headache- more subarachmoid hameorrahge
headache
nausea
vomiting
stiff enck
nyastamus
11
Q
on examination how would ypu examine a pt wiht suspected stroke
A
focused neuro exam
vitals- bp, saturation, hr
FAST
cv- got any arrhtmia murmurs. pulmoanry odedmea, heart failure
12
Q
what differential diagnosis are there for signs and symptoms that are stroke like
A
hypoglycemia!!!
alchol / drug toxicity
dizzy condtions=> syncope, labrythine disroders= menieres disease, vertigo, labyrthinitis
neuro =
sizures
migraine with aura
demyelineation- ms
peripheral neuropahty
spinal epidural haematoma
trauma
infection=
sepsis
encephalitis
cns abscess
encephalopathies=
wernickes encephalopthy
hypertenisve encephalopathy
others=
dementia
acute confucsional state
vasculitis
somatoform/conversion disorder
13
Q
how do you manage a suspected stroke
A
exclude hypoglycemia
immediate brain CT
once had CT and not haemorragic give 300mg aspirin stat then for 2 weeks
if ischmic = thrombolysis with alteplase = can do within 4.5 hrs
thrombectomy within 24 hrs if accesible
if over 4.5 hrs five 300mg asprin OD for 14 days. if asprin contraindicated give clopidogrel
stroke rehab
14
Q
whats tia managemnt
A
secondary prevention
aspirin 300mg
see specialist within 24 hrs
do ABDC2 score to see risk of having stroke within 48 hrs
15
Q
what imaging do you do for suspect stroke / tia
A
Diffusion weighted MRI = gold standard
or CT
carotid us TO ASSES IF CAROTID STENOISS
16
Q
what do you do if ther eis carotid stenosis on US
A
endarterectomy pr carotid steniting
17
Q
what can you do for secondary prevention for stroke/tia
A
75mg OD clopidegrel or if not ok then use dipyrimdamole 200mg BD
atorvastatin 80mg - dont start immediately
carotid endarectomy / stent if got carotid stenosis
treat modifiable facotrs= ht, diabtetes, smoking, af, diet, alcohol etc
18
Q
if someone has a stroke/tia can they drive
A
no need to infrom dvla. look on cks website about how long cant drive for etc
19
Q
whats the percentage of harmoragic stroke
A
10-20% of strokes are intracranial bleeds
20
Q
whats the types if intraranial bleeds
A
extradural
subdural
subarachnoid
intracerebral
21
Q
whats the risk factors/causes of burstin a blood vessel and causing a haemorrhagic stroke
A
hypertension
anyerusm
ADPKD
head injury
old
alcholic
ischemic strokes can progress to haemorrhagic
brain tumours- have own bv that arnt as good
anticoagulants -warfarin
22
Q
sudden onset headache is a key sign of what
A
haeorhagic stroke
23
Q
whats the s and s of haemorhagic stroke
A
sudden onset of headache
vomiting
seizures
neurological aytmpoms
weakenss- fast
reduced consiousness
24
Q
a patient has a gcs of 8/15. what do you need to start to consider
A
do they require secruing the airway open- ventilation, intubation, icu ?
8 and below thinji airway
25
on a ct scan there is a crescent shape. and the shape isnt limited by cranial sutures
what is this
subdural haemorrahge
26
what causes subdural bleeds
bridging veins rupture
27
an alcholic hit his head - minor- and felt funny but then was fine. later on he lost consiouness, was sick and felt dizzy and diffifuclt to speak . what is this
subdural haemorrhage
the symtpms can come on quick if severe head injury
28
who are commonly to have subdural haemorrahes and why
elderly and alcoholics
brain atrophies and briding veins are strethced so more easily rupture
29
whats the common artery to rupure in extra dural haemorahge
middle menigeal artery
30
what does extra dural hameorahge look like on ct
bi convex and limited bu crnaial sutures
like half a lemon- pushes into the brain (its a bit extra it wants to show itsslef and its a bit fat so round where as subdrual are sub so they half and skinny so crescent shape)
31
a patient fractures his temoral bone what arteyr may be affects and waht can this lead to
middle menigela artery may have been ruptured leading to a extra dural haemorrahge
32
a young paitent has a traumatic head injury and has an ongoing headache
he has a period of imprive neruo symtpoms and consiousness but then he rapidly declines over few hrs
what is the cause
extra dural haemroage
33
how does an intracerebal haemorage present
similar to ischemic stroke
sudden onset
34
why do intracerebal haemoeages occur
spontaneous
anyrsm rupture
tumour
bleeding due to an ischemia infarct
35
a patient was lifiting a weigh / having sex and he suddenly got a realy awful headache at the bacl of his head like being hit by a brick so sudden
what is this
subarachnoid hameorraghe
36
whats the casue of subarachnoid haemrroage
cerebal anyurseum rupture
37
what can subarachnoid hameorages be associated with
cocaine use
sickle cell aneamia
38
how do you manage an intracranial bleed
immediate ct see what cause
FBC and clotting
stroke unit
recued hypertension but avoid hypotension- brian needs o2
correct clotting abnormality
consider intubation, ventialtion, icu if 8 and below gcs
39
find blood in the CSF what haemoragic stroke is this
subaracnoid
this is where the csf is in the subaracnhoid space
40
whats the major symtpom of subarachnoid ahemorrage
sudden onset of v painful occipital headache
= thurnde clap
= hit on back of head
41
where is the bleeding in a subarachnoid haemorrhage
between the pia mater and arachnoid matre= in subarachnoid space
42
what is n the subarachnoid space
csf
43
patient has
thunderclap headahce sundenly come on whilst lifting weights
stiff neck
photophobia
has some visual changes, speech changes and then has a seizure
and looses consuoisness
what is this
subarachnoid hameorrhage
44
whats the riskk factors of subarachnoid haemorrahge
smoking
hypertension
excessive alchol use
cocaine use
fam hist
asiccoated with:
cocaine use, sickle cell anemia, connective tissue disorders= marfans sundrome, ehlers-danlos, neurofibromatosis
more commen in black pt, women, 45-70
45
what investigations do you do if pt has v bad sudden onset occipital headache, stiff neck, ohotophibia, vision gone blurry
subarachnoid haemorrhage=
ct head immediately
if negative then do lumbar puncture if do suspect it
once subarachnoid haemorrhage confirmed do angiography ct/mri to find source of bleeding
46
a patient has a lubar puncture and fine raised red cell count in the csf and its yellow
the patient has a sudden onset occiital headache
subarachnoid haemorrhage= in csf cus in same space get raised red cells in the csf and the csf goes yellow because billirubin in csf= xanthochromia - billirubin by product of red blood cell
47
what managemnt is there for subarachnoid haemorrhage
if dec consiousness inutbtion and ventialtion
MDT - everyone involved, nutrtion, ohysio etc
surgical intervention to treat anyerusm- coiling (catheter) or clipping (cranial surgery)
nimodipine = ccb to prevent vasospasm which is a complication of a subarachnoid heamorrage that would cause ishcemia to the brain
lumbar puncurue or shunt t treat hydrocephalus if there
anti epileptics for seixures
48
whats a common complication of subarachnoid haemorrhage
vasospasm causing ishemia to the brain
49
whats this
intense pain around one eye. Attacks occurs once a day, each episode lasting 1 hour for the past 8 weeks. Associated with a red and watery eye and a constricted pupil
Cluster headache
50
constant headache with nausea worse in the morning and on coughing suggest what
raised intracranial pressure
51
decreased GCS
headache
nausea and vomiting asociated with what
haemorrhagic stroke
52
what drug is most commonly first line used to to terminate acute seizures
benzodiazapines
52
how do you treat trigeminal neuralgia
carbamazepine - first line
surgery to decompress the nerve or can intentionally damage the nerve
53
a patient comes with a headache. what are all the differentials is could be
cluster heaache
tension headache
hormonal headache
analgesic headache
secondary headache
sinusitis
raised intra cranial pressure
brain tumour
giant cell arteritis
glaucoma
intracranial hameorrhage
subarachnoid haemorrhage
carbon monoxide poisoning
meningitis
encephalitis
trigeminal neuralgia
cervical spondylosis
migraines
54
whats the red flags you need to ask for headache
fever, stiff neck?= menigitis/encephalitis
ne neuro symptoms?= stroke, haemorrhage, malignancy
dizziness?= stroke
visual disrurbance?= glaucoma, stroke, giant cell arteritis
sudden onset occipital headache?= subarachnoid haemorrhage
worse on coughing/straining/ in morning?= raised intracranial pressure
vomiting?= raised intra cranial pressure, co poisoning
postural/ worse on stadning, worse lying, benidng over= raised intracranial pressure
severe enough to wake up from sleep?
jistory of trauam= intracranial haemorrhage
pregancy?- last 6 months?- pre-ecampsia
55
when do you need to consider pre eclampisa when a pt has a headache - what stage in pregancy
if got headache in second half of pregnacy investigate for pre-eclampsia
56
patient has mild ache across forehead which is band like that comes on gradually
tension headache
57
what signs and symptoms of tnesion headache
band like
mild ache across forehead
no visual disrubance
come on and resolve gradually
58
what associations are there with tension headaches
dehydration
alcohol
stress
depression
skipping meals
59
what treatment for tension headache
simple analgesia
reassurance
warm towel to area
relaxtion techniques
60
what headaches have stumpoms like a tension headache- band like across forehead mild ache gradual onset
horomonal headache
analgesia headahce
secondary hedaches
61
whats secondary headaches
tension headaches with clear cause
- alcholol
head injurt
CO poisoning
medical condition- infection, pre eclampisa, obstructive sleep apnoea
62
a patient has a headache,
they have facial pain over the eyes, nose and forehead
its tender to touch over the cheek bone they say
what is this
sinusitis- tneder to touch over sinus area is giveaway if they have this
resolves 2-3 weeks
63
is sinusitis mainly viral or bacterial?
viral
64
what treatment for sinusitis?
nasal irrigation with saline
if prolonged symptoms - over 2-3 weeks should have reoslved- then nasal steroid spray
antibiotics occasionally
65
what is sinusitis
headache with inflammation of one/more sinuses
66
a patient has a band like headache that they keep having for ages
they have been taking pain killers ofr over 3 months for aches and pains of their body and now for the ehadache too
what is this
analgesia headache
= long term analgesia use/excessive use
treat by withdrawing from alagesia- reasure pt that its the analgeisa that is causing the pain
67
a female patient comes in becasue she keeps having refular headaches. they happen about 2 days before her period and then for the forst 3 days of her period but it then stops. what is this
hormonal headahce
68
what the cause of hormonal headaches
low oestrogen
69
whats the s and s of hormonal headaches
2 days before period and first 3 days of period have the pain
generic non specific- tension like
may ne going through the menopause/pre menopausal
can get it in first few weeks of pregancy but will improve over last 6 months
70
a patient is pregant and keeps getting headaches. shes in her first 4 weeks in
shpuld you be concerned about pre ecalmpsia?
no.
be concrned if headaches in last half of pregancy
71
patient is preganct and is getting headaches that are getting worse and shes 6 months into pregancy
should you be worried?
yes. considere pre eclampsia
headaches in forst few weeks that get better in last 6 months are hormonal headaches. if get worse or get headaches in last half of pregancy then investigate for pre ecampsia
72
how do you treat hormonal heaaches
contrceptive pill can help
HRT
if getting the headaches when off the pill in the week off can have packs back to back to help
some people find that pill can make them worse though
73
a patient has a headache and neck pain. what could this be? and need to exclude?
could be cervical sponylosis but need to exclude:
inflammatory, maligancy, infection, spinal cord/nerve root lesions
74
whats cervical spondylsosis
degenrative changes of the cervical spine
75
a patient has intense facial pain on one side of his face ocver his cheek and to the ear and down to the jaw. feels like electricity shooting. sometimes last seconds sometime shours but it seems to be getting worse
trigeminal neuralgia
76
whats trigeminal neurlagia and the s ans s
can affect combo of branches
cause isnt certain but could be due to compression of nerve
90% are unilateral
5-10% of patients with multiple sclerosis ahve this
intense pain - like electricity shooting
spontaneous
can last seconds - hrs
attacks often worsen in severity over time
triggers can be cold weather, citrus fruit, spicy food, caffeine
77
what triggers can casue trigeminal neuralgia
cold weather
spicy foods
caffeine
citrus fruit
78
how do you treat trigeminal neuralgia
carbamazepine - first line
surgery to decompress the nerve or can intentionally damage the nerve
79
a patient comes with a headache. what are all the differentials is could be
cluster heaache
tension headache
hormonal headache
analgesic headache
secondary headache
sinusitis
raised intra cranial pressure
brain tumour
giant cell arteritis
glaucoma
intracranial hameorrhage
subarachnoid haemorrhage
carbon monoxide poisoning
meningitis
encephalitis
trigeminal neuralgia
cervical spondylosis
migraines
80
whats the types of migraine
migraine with aura
migraine without aura
silent migraine- no headahce just aura
hemiplegia migraine
81
whats s and s of migraine
headache an last 4-72hrs
moderate to high interensty
pounding/throbbing
usually unilateral
photophobia
phonophobia
with/without aura
nausea and vomiting
aura= visial changes
blurred vision
sparks in vision
lines across vision
loss of different visual fields
82
whats the stage of migraine
not all pt have all 5 and vary
prodromal = can being 3 dyas before headache- yawn, fatigue, mood changes
aura- lasts up to 60 mins
headahce- last 4-72hrs
resolution- fades and can be relived by vomiting/sleeping
recovery/postdromal
83
what triggers can casue migraine
vary
can be har d to identify
stress
dehydration
certain foods-caffeine, chocolate, cheese
mesturation
abnormal sleep patterns
trauma
birhgt lights
strong smells
84
what acute managemnt can a patient have when expeirivning migraine
dark room and sleep
paracetamol
NSAIDs= naproxen, ibruprofen
antiemetcis if vomiting- metaclopramide
triptans - sumatriptan 50mg as migrain starts
85
what do triptans do that could help with migraine
act on smooth muscle of arteries and casue vasoconstiction
inhibit pain receptors
decrease neuronal acitivty in CNS
86
what prophylaxis can be done for migraines
propanolol
topiramate - teratogenic!!
amitriptyline
if migraine triggered by menstruation then can use triptans or NSAIDs = mefanamic acid
frovatriptan / zolmitriptan
87
what drug do you use for prophalxis of migraines that is teratogenic
topiramate
88
red swollen watering eye
nasal discharge
facial sweating
severe pain around eye
what is this
cluster headache
89
whats s and s of cluster heaache
get cluster of attacks then non for a while
red, swollen, watering eye
nasal discharge
intolerable exrely sever epain usually around eye
typically unilateral
miosis
ptosis
facial sweating
attacks last 15 mins to 3 hrs
90
what triggers can there be of clustr headache
alchol
strong smells
exercise
91
what treatment is there for pt exeprinceing a cluster ehadache
triptans- sumatriptan 6mg injected subcutaneously
high flow 100% oxygen for 15-20 mins- can be done at home
92
what prophylaxis is there for cluster headaches
varapamil
lithium
prednisolone - 2-3week course to try and break the cycle in the cluster
93
what happens in brown-sequards syndrome
unilateral spastic paresis and loss of proprioception/vibration sensation with loss of pain and temperature sensation on the opposite side
94
whats this
bilateral spastic paresis and loss of pain and temperature sensation
anterior spinal artery occlusion
95
whats a benign essential tremor
fine tremor affecting all voluntary musclees
96
where can the fine tremor be seeen in benign essentail tremor
commonly in hands but can the tremor in head, jaw, vocal temor
97
whats the features of benign essential tremor
5-8hertz
associated with older age
worse on voluntary movment- imporves wit rest
worse when tired, stressed, after caffeine
improves with alcohol
absent during sleep
98
what do you need to exclude before clinically diagnosing benign essential tremor
parkinsons
huntington chorea
ms
hyperthyroidism
fever
med- anti psychotics
99
how do you manage beningn essential tremor
only give med if causing functional/ pscyholigical problems
propanolol - non selective beta blocker
primidone - barbituate ant epipleptic
100
whats the difference between benign essential tremor and parkinsonian tremor
PT, 4-6hertz= BT 5-8 hertz
PT, worse at rest= BT improves at rest
PT asymmetrical = BT symmetrical
PT imrpoves with intentional movement = BT worse with intentional movement
PT other parkinson features =BT no parkisnon features
PT does not change with alcohol = BT improves with alcohol
101
a patient is 70
they have a tremor
they pick up a cup of tea and the tremor in that hand worsens
they sometimes have a beer in the evening which helps the tremor a bit
what is this
benign essential tremor
102
whats parkinsons
progresive reduction of dopamine in the basal ganglia causing disorders of movement
103
what neurotransmitter is lacking in parkinsons
dopamine
104
where does dpoamine get produced
substantia nigra
105
whats the signs and symtpoms of parkinsons
resting tremor
bradykinesia
rigidity - cogwheel
bradykinesia= slow movements that get slower and smnaller
handwriting gets smaller and smaller
shuffling gait
hard to inititate movement
difficult to turn around when standing
hypomimia - mask like face
tremor usually asymmetrical - one side worse than other
depression
sleep disrubance and insomnia
postural instability - hypotension makes thi worse and increased risk of falls
cogmitive impairement and memory problems
106
what parkinsons - plus syndromes
dementia with lewy bodies
multiple system atrophy
progressive supranuclear palsy
corticobasal degeneration
107
what signs and symtpoms are there with lewy body dementia
parkinsonism features
progressive cognitive delcine
visual hallunciations
disturnaces with rem sleep
fluctuating consiousness
delusions
108
whats multiple system atrophy
parkinson features
where neurones of multiple systems degenerate
have also autonomic dysfucntion= postural hypotension, consitpation, abnormal sweating, sexual dysfunction
cerebellar dysfucntion= ataxia
109
what management is there for parkinsons
levodopa = synthetic dopamine
- try use last as efectiveness wears off over time
use a peripheral decarboxylase inhibitor with levopdopa to stop it being broken down before get to brain - carbidopa and benserazide
= co-careldopa
= co-benyldopa
COMT inhibitors = entacapone take with the combo of levodopa and pdi to extend effectiveness of leveodopa
dopamine agonist = bromocryptine, pergolide, carbergoline
use to delay use of levodopa then use with levodopa to reduce dose needed
mao b inhibitors = specifiv to dopamine
use on own and then with levodopa to recduce dose of levodopa needed
= selegiline, rasagiline
110
whats the side effects of leveodopa
dyskinesias due to too much dopamine
dystonia = excessive muscle contraction=> abnormal posture, exagerated movement
chorea= abnormal involuntary movements - jerking and random
athetosis= involuntary twisting/ wrtighing movements usally in fingers, hands and feet
111
entacapone is what type of drug and use when
comt inhibitor used in parkinon treatment
112
co-benyldopa is what and used when
levodopa and benserazide used in parkinsons treatment
113
bromocryptine
pergolide
carbergoline
what drugs are these and used when
dopamine agonsots used in parkisnons treatment
114
what side efect of dopamine agonsits are there
pulmonary fibrosis
115
a patient has parkinsons disease and also pulmonary fibrosis
what could be the cause of the pulmonary fibrosis
medication
dopamine agonist
116
selegiline
rasagiline
what drugs are these and used when
MAO b inhibitors
parkinson treatment
117
whats neuropathic pain
caused y abnormal functioning of the sensory nerves delvering abnormal and painful signals to the brain
118
whats paresthesia
burning, tingling, oins and needless and numbness
119
whats the signs and symptoms of neuropathic pain
burning
tingling
pins and needles
electric shocks
loss of sensation to touch of afected area
120
what investgation can be done if suspect neuropathic pain
DN4 questionaire
asses character of pain
score 4 over
121
whats the causes of neuropathic pain
post herpetic neuralgia = shingles
in distribution of dermatome
nerve damage from surgery
MS
diabetic neuralgia- esp foot
trigeminal neurlagia
complex regional pain syndrome
122
whats complex regional pain syndrome
area ffected by abnormal nerve funcioning
causes neuro[athic pain and abnormal sensation
usually isolated to one limb
often triggered by injury to area
can be very painful- even wearing clothes can hurt
can intermittently swell, change colour, change temp, flush and abnormal sweating
123
whats the management of neuropahtic pain
amitriptyline
duloxetine
gabapentin
pregabalin
these are frist line so use one then if doesnt work use another - except trigeminal neuralgia is carbamazapine first line
other options
tramadol- ony use toshort term to try control flares
capsaicin cream - to localised area
phsyio.- maintain strength
pschycological - understanding and coping
124
whats motor neurone disease
progressive degeneration of motor neuones both upper and lower - no sesnory symptoms
125
whats the most common type of MND
amylotrophic lateral sclerosis
126
whats the second most common type of MND
progressvie bulbar palsy
127
whats the types of mnd
how they present
Amylotrophic lateral sclerosis
progressive bulbar palsy
primary lateral scleorisis
progressive muscular atrophy
128
whats risk facotrs for mnd
fam hist of it
smoking
exposure to heavy metals
certain pesticides
129
whats this
60 year old man with progressive weakness throughout his body
keeps tripping on things
slurs his speech a bit
MND
130
whats the possible presentatios of mnd
weaknes of msucles throughout body
weakness usually first noted in upper limbs
slurred speech
increased fatigue when excerising
tripping/clumsy/dropping things
stiff/cramp
muscle wasting, fasciculations, reduced reflexes, reduced tone= lmn
increased tone/spacitisity, brisk reflexes, upgoing plantar relfex= umn
131
how to manage mnd
support fam and pt= MDT, break bad news well, advaned directives to document pts wishes, end of life planning
riluzole= can slow progression and extend survival in AML
NIV- help breahting at night
132
what investigations do you do if suspect mnd
excluded other causes of motor neurone issues
clinical diagnosis by specialist
133
what medication do you give for bells palsy within 72hrs of symptom onset
corticosteroid- prednisolone
134
whats ms
chronic progressvie condition
demeylienation of CNS neurones
immune mediated inflammatory condition
135
32 year old woman
double vision for few weeks thrn went
now got numbness in right arm
gets headaches that are over the right jaw and right top head
what is this
MS
neurological signs= trigeminal neurglagia is last thing
136
whats signs and symptoms of MS
symtpoms usually progress over 24 hrs
early on in disease the symptoms fully resolve later on become more permanent and symptoms worse
stymptoms last days to wees intitally
optic neuritits
eye movement abnormalitites= internuclear opthalmoplgia
conjugate lateral gaze disorder
(look laterally in direction of affected eye and the affected eye wont abduct)
focal weakenss: bells palsy, horners syndrome, limb paralysis, incontinence
focal sensory symptoms: trigeminal neuralgia, numbness, paraestheisa, postive lhermittes sign
cerebellar- ataxia,, vertigo, clumsiness, dysmetria
sensory ataxia- positive romberg test and gait disturbance
137
how can ms be descirbed in patterns
relapsing and remitting -active and / worsening
secondary progressive - starts off relapsing and remitting then worsens and symptoms dont fully resolve- incomplete remissions
primary progressive
- active and/progressing
138
how manage relapse of ms
methylprednisolone 500mg oraly daily for 5 days
or iv 1g daily 3-5 days if severe
manage symtpoms
exercise
neuropathic pain- gabapentin/amitriptyline
depression- SSRI
urge incontinence- tolterodine/oxybutyrin
spasiticity- physio/ gabapentin/ baclofen
139
investigations for ms
lumbar puncture- oligocolonal bands in csf
mri see lesions
140
causes for ms
vit d deficiency
smoking
obesity
EBV
genes
141
what age and gender get ms
female
20-50s
142
whats a v common sign/symptom of ms
optic neuritis
143
s and s optic neurtis
unilateral reduced vision
develop over hrs - days
central scotoma- enlarged blind spot
pain on eye movment
impaired colour vision
relative afferent pupillary defect
144
es of opitic neuritits
ms- most common - 50% get optic neuritis likkely develop ms
diabetes
siphilis
measles
mumps
lymes disease
sle
sarcoidosis
145
treatment opitic neurtits
steroids
2-6 week recovert
146
eye drooping and mouth drooping on left side of face
what nerve is affeced and upper or lower?
left sided lower motor neruone
facial nerve
147
how do tyou know if its upper motor neruone ornmlower motor neurone in facial nerve pasly
upper motor neurone the forehead is spared
lower motor neurone all the face affeted
upper facial nucleus has bilateral innervcation from both sides of brain
lower facial nucleus has contrlateral innervation
if stroke on right side of brain
the left side of lower half will droop and spare left forehead cus the top left forehead is innervated also by the left side of the brain too
148
rash round ear and unilateral drooping of mouth and eyes and forehead
what is this
ramsay hunt syndrome
149
what innervation does the facial nerve supply
motor= facial expresion
stylohyoid
platsyma
stapedius of inner ear
posterior digastric
sensory= anterior 2/3 tast of tongue
para= supply para to sublingual and submandibular glands and lacrimal gland
150
whats bells palsy
idiopathic
unilateral lmn facial nerve pasly= enitre side of face affected - same side of lesion
151
treat bells pasly
within 72hrs of onset can give prednisolone - 50mg for 10 days or 60mg for 5 days then 5 day of reducing by 10mg each day
lubricating eye drop give no matter time
most will get better several weeks some take a year to get better
- 1/3 have lasting weakness
152
whats the cause of ramsay hunt syndrome and whats and s
herpes zoster virus
unilateral lmn facial nerve pasly- affect entire side of face
vesciular rash around ear / in esr canal/ pinna. can extend to anterior 2/3 of tongue and hard patlate
rash same side as affectedface
153
treat ramsay hunt syndrome
initiated within 72hrs
prednisolone and
aciclovir
lubricating eye drops
154
what causes are there of lmn lesion causing facial nerve palsy
bells palsy- idiopathic
ramsay hunt syndrome- herpes zoster virus
infection= otitis media, malignat otis externa, HIV, lymes disease
systemic= diabetes, sarcoidosis, MS, lukaemia, guillian barre syndrome
tumors= parotid, acoustic neuroma, cholesteatoma
trauma= direct nerve trauma, damage in surgfery, base of skull fracture
155
where does the facial nerve leave the skill and what does it go through
exits at brainstem at cerebellopontine angle
passes through temporal bone and parotid gland
156
whats the branches of the facial nerve
temporal
zygomatic
cervical
buccal
marginal mandibular
157
whats presentation of brain tumours
neurological symptoms to location
signs and symptoms of raised intracranial prssure
158
erson has headaches thats be continuous for 4 days and its worse when they wake up
what could this be a sign of
what simple test can you do
raised intracranial pressure
measure bp - ht?
fundoscopy- look for papilloedema
159
signs and wymptoms of raised intracranial pressure
papilloedema
headaches--> constatn
nocturnal
wonrse on waking
worse on coughing, straining, leaning forwards
vomiting
altered mental state
visual field defect
sizures- esp focal
unilateral ptosis
cranial nerve 3 and 6 palsies
160
whats the types of brain tumours
metasates from lung, breast, colorectal and prostate
gliomas= tumout of glial cells
these are graded 1-4
4 being most maligant
astrocytoma- glioblastoma multiforme most malignant
oligodendroglioma
ependymoma - benign
meningiomas- usually benign but bad cus raised icp
acoustic neuroma= tumour of schawann cells aroud the auditory erve of the inner ear
pituiatary tumours
161
sign and symptoms of acoustic neuroma
occur at cerebellopontine angle
slow growing
usually unilateral
hearing loss
tinnitus
balance problrms
cn 7 pasly
162
if aucstic neuroma is bilateral what type of tumour is it
neurofibromatosis type 2
163
signs and symptoms of pituitary tumour
bitemporal hemianopia
hormone deficiences or hormones in excess-->
acromegaly= inc GH
hyperprolactinaemia = inc prolactin
cushings disease = inc ACTH and cortisol
thryotoxicosis= inc TSH and thyroid hormone
164
treat pituitary tumour
transphenoidal surgery
radiotherpay
meds to supress if excess hormones=
somatostatin analouges if excess GH= ocreotide
bromocriptine to block prolactin secreting tumours
165
whats huntingtons chorea
autosomal dominant progressive degenration of neurones
166
whats the cause of huntingtons chorea
autosomal dominant
trinucelotide repeat disorder of the HTT gene on chromosome 4
shows anticipation - each sucesssive generation has increased repeatitions and so has early age of onset and increase severity of symtpoms
CAG repeats
167
hats anticipation
a feature of trinucelotide repeat disorderes
each sucessive generation has increased repeats of the gene and so increase severity of disease and earlier age of onset
168
30 yr old
has progressive worsening of symtoms
habing mood changes lots
then started having movement problems where was making involutary movements and struggling to swalloe
what is this
huntingtons chorea
169
s and s of huntingtons chorea
gradual and progressive symotms
starts around 30s-50s
starts with cognitive (including demetia) , pscyiatric, mood disorders
then moves onto movement disorders
chorea= abnormal andinvoluary movements
dysarthia= issue speaking
dysphagia
eye movement disorders
behavioural problems - issues with family, job loss etc
170
diagnosis of huntingtons
genetic testing
have pre and post counselling
differnetials- other causes of dementia
other causes of chorea
171
treatment for huntingtons
no tratment just symtpomatic relief
MDT
speech and language therapy if needed
genetic cousnelling for fam, preg, childnren
adavance directives
plan end of life
supress movement disorders= antipsycotics- olanzapine
benzodiazapines= diazapam
dopamine depelting agents= tetrabenazine
172
whats cause of death and life expecatncy in huntigtons chorea
suicide more common
often other ilnnes =cus more suspetible to illness= pneumonia
life expectancy 15-20yrs after onset. ofsymptoms
173
whtas myasthenia gravis
autoimmune condition that casues muscle weakness that gets worse on muscle use and improves with rest
174
cause of myasthenia gravis
strong link between thyoma and this
AchR antibodies= bind to ach r at nmj and so ach cant bind so cant stimulte r so cant illicit muscle contraction
10% of patietns due to MuSK auto antibodies
5% of patients due to LRP4 auto antibodies
last 2 auto antibodies are for proteitns that are respo sible for creaition and organisation of Ach r = not enough AchR
antibodies can also activcate complement system in the nmj and so damage the cells at the post synaptic membrane
175
patiet has LRP4 autoantibodie
what does this cause
or
patient has MuSK antobodies
mysathenia gravis
176
whats s and s of myasthenia gravis
muscle weakness worse in evening
women under 40
men over 60
thyoma
mostly affects proximal muscles and muscles of head and neck =
extraocular m weakness= diplopia
eyelid weaknes= ptosis
diff swallowing
fatige in jaw when chewing
weakness in facial movements
slurred speech
177
what can you do on examination to test for myasthenia gravis
want to elict muscle fatiguiability
repeated blinking- can exaserbate ptosis
prolonged upward gaze can ellicit diplopia
repeated abduction of arm 20 times then when compare find unilateral weakness to that arm
check to see if thymectomy scar
test FVC
178
how to diagnose myasthenia gravis
antibodies test- AchR antibodies
LRP 4 antibodies
MuSK antibodies
ct/mri of thymus gland to look for thyoma
edrophonium test- give IV edrophonium chloride/ neogstimine = this blocks acetylcholinesterase so more ach in the nmj so more availble. tobind to temporaily and briefly relives weakness
179
what certainly estabilsh a diagnosis of myasthenia gravis
edrophonium test
180
what treamtent is there. for myasthenia gravis
neostigmine/ pyridostigmine = achesterase inhibitors
prednisolone/ azathioprine = supress antobody production
thymectomy= even if no thyoma can help
rituximab if nnothing else works- monoclonal ab agaisnt b cells
181
patient has sudden inability to breath they have had an upper resp trsct infection and are on neostigmine
what is this
myasthenic crisis
have myasthenia gravis and have acute worsening of symptoms often trifgfered by another illnes eg. upper res tract infecction
can casue resp failure as the resp muscles weaknes
give niv/ bipap/ intubation/ ventilation
give immunomodulatory therapy= iv immunoglobulins and plasa exchange
182
whtas lamber eaton myasthenic syndrome
similar to myasthenia gravis
autoimmune agaisnt voltage gated calcium channels.
183
whats the casue of lambert eaton myasthenic syndrome
antibodies agasint voltage gated calcium channels
these are in presynatoic termials of nmj and so the channels are destroyed so less Ach can be released into the synapse
VGCC are found. in small cell lung cancer so antibodies produced= small cell lug cancer major casue
184
if patient has lambert eaton myasthenic sydrome what do you need to consider to investigate for
small cell lung cancer
185
signs and symptoms of lambert eaton myasthnic syndrome
slower pregression and less pronounced symtoks of myasthenia gravis
proximal muscles affected most- gait affected more than in MG (mg is more face issues)
weakness increased with prolonged use (although some say can have improvement) - worse in evening
ptosis
diplopia
slurred speech
dysphagia
186
what investigations of LEMS
ct/mri to see if malignacy the cause - consdier small cell lung cancer esp if older smoker with symtpoms
VGCC antibodies
screen for underlying malignacy after 2 years of diagnosis of lambert eaton myasthenic syndrome
187
treatment for lambert eaton myasthenic syndrome
amifampridine = blocks voltage gated potassium channels in presynaptic termianl of nmj = prolongs depolarisation = ca channels able to work more= increased acetylcholine releasd into synapse
immunosupressants= prednisolone/ azathioprine
iv immunoglobulins
plasmapheresis
188
what casues are there of peripheral neuropathies
charcot marie tooth disease
A- alcohol
B- B12 deficiency
C- cancer and CKD
D- diabetes and drugs- isonazid, amidarone, cisplatin
E- every vasculitis
thyroid disease
infection - hiv, syphilis, leprosy
189
whats chacot marie tooth disease
iheirted peripheral neuropthy- motor and sensory
vasrious types of it
most genetic mutations are autosomal dominant
causes dysfunction to mylein or axons
mutations can arise. denovo
190
high foot arch
bilateral foot drop
reduced tendon relfexes
peripheral sensory loss
symmetrical atrophy to the muscle below the knees - inverted champage bottle legs
charcot marie tooth disease
191
s and s of charcot marie tooth disease
slowly progressive
weakness of feet and anles
depressed or absent tendon relfexes
weakness of dorsiflexion
bilateral foot dtop
symmetrical atrophy of muscles below the knees- inverted champagne bottle legs
atrophy of muscles of hands- esp thenar muscle
high foot arch- pes cavus
weakness in lower legs
weakness in hands
decreased muscle tone
peripheral sensory loss
192
what ages does charcot marie tooth disease present
before 10 usulay
can be delayed to age 40 though
193
what investigfations to do for susepcted charcot marie tooth disease
mri/ct of brain and sc
exclude other neuropathies- blood test for b12, folate, lft, ck, antinucelar ab
muscle biopsy
csf
nerve conduction studies - can show got cmt disease
194
managemnt of charcot marie tooth disease
supportive
orthopdeics
podiatrist
ot
physio
neuro and geneticits for diagnosis
195
patient has sudden onset of weakness in both feet and now in lower legs
had a tummy bug 3 weeks ago
what is this
guillain barre syndrome
196
whats guillain bare syndrome
scute paralytic polyneuropathy affectig periperal nervous sytem = autoimmune demyelination and axonal degenration
197
cause of guillain barre syndrome
molecular mimicry =
have infection so b cells produce antibodies agaionst antigen of pathogen
thieese antiboides also match for protiens in nerve cells - mylien sheath, axon
get degenration. ofthe nerves
198
what infections are strongly linked to guillain barre syndrome
camplyobacter jejuni
cytomegalovirus
epstein barr virus
199
signs and symptom of guillain barr syndrime
hypotonia
symmetircal ascending weakness starting in feet and moving up body - can also start in hands and move up
redcued relfexes
can have periperal loss of sensation
can have neuropathic pain
can progress to cranial neres-> facial nerve pasly (all of face)
can in sevre cases get resp failure due to paralysis. of resp muscles
200
when do symtoms of guillain barre syndrome start
within 4 weeks of previous infection
symptoms peak at 2-4 weeks and then recovery period is motnhs - years
201
how to diagnose guillain barre syndrome
lumbar puncture- csf have high protein, normal gluocse and cell count
nerve condcution studies- redcues signal
think other casues ofacute paralysis
202
what casues are there of acute apralysis
guillain barre syndrome
brain- stroke, encephalitius, brainstem compression
sc- sc compression, infection
anterior horn cell= enterovirus, poliovirus
nerve root- CMV, HIV
peripheral nerve- vasculitis, lead poisoning, lyme disease, thyamine def, diptheria
nmj= myasthenia gravis(more slow though and worse when moving ), lambert eaton myastheinc syndrome, botulism
muscle- hypokalemaie, polymyositis
203
management of guillain barre syndrome
iv immuoglobulins
plasma exchange
suportive care
vte prophylaixis
204
hats a leading cause of death in guillain barre dynsrome
PE
205
hat medication is given for men with epilelpsy
* generalised seizure: sodium valproate
focal seizure: lamotrigine or levetiracetam
206
How does cushings syndrome casue hypokalaemia and metabloc alkalosis
high cortisol can act as a mineralcoritcioid
potassium is therofre excreted as na reabsorbed
hydroen ions swapped for na so secrete h ions
So get cushing sydnrome features and muscle cramps, tremor, weakness = hypokaelmiea
207
How does cushings syndrome casue hypokalaemia and metabloc alkalosis
high cortisol can act as a mineralcoritcioid
potassium is therofre excreted as na reabsorbed
hydroen ions swapped for na so secrete h ions
So get cushing sydnrome features and muscle cramps, tremor, weakness = hypokaelmie
208
whats the cushing reflex
bradycardia and hypertension
The Cushing reflex is a physiological nervous system response to increased intracranial pressure that results in hypertension and bradycardia. Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) - intracranial pressure. Therefore if intracranial pressure is high, the only way the body can compensate to increase CPP is by increasing MAP. A sympathetic reflex therefore results in hypertension. This results in a counter parasympathetic reflex by stimulation of the baroreceptors resulting in bradycardia.
Bradycardia and hypertension with a wide pulse pressure is the correct answer. Cushing's triad, compromised of widening pulse pressure, bradycardia and irregular breathing, is a late sign indicating impending brain herniation. Systolic hypertension occurs as a reflex to maintain cerebral perfusion pressure in the presence of raised intracranial pressure.
209
ptient hit laterally in head with cricket ball
what worry about
The mechanism of injury, loss of consciousness and 'lucid interval' should ring alarm bells for an extradural haematoma.
210
water deprivation test of primary polydipsia show what
Water deprivation test: primary polydipsia
urine osmolality after fluid deprivation: high
urine osmolality after desmopressin: high
211
whats the difference in primary polydipsia and dehydration in water deprivation test
Dehydration . This patient would have a high urine osmolality to begin with and he is not clinically showing signs of dehydration (e.g. dry mucous membranes and prolonged capillary refill time) based on the hydration status assessment. Further investigations would also be needed to assess the cause of his dehydration as he is drinking water and it is not addressing his thirst.
212
what would high stepping gait indicate
A high-stepping gait develops to compensate for foot drop. If found unilaterally then a common peroneal nerve lesion should be suspected. Bilateral foot drop is more likely to be due to peripheral neuropathy.
213
A 64-year-old female with a history of rheumatoid arthritis presents with increased difficulty in walking. On examination there is weakness of ankle dorsiflexion and of the extensor hallucis longus associated with loss of sensation on the lateral aspect of the lower leg. What is the most likely diagnosis?
common peroneal n pasly
The sciatic nerve divides into the tibial and common peroneal nerves. Injury often occurs at the neck of the fibula
The most characteristic feature of a common peroneal nerve lesion is foot drop.
Other features include:
weakness of foot dorsiflexion
weakness of foot eversion
weakness of extensor hallucis longus
sensory loss over the dorsum of the foot and the lower lateral part of the leg
wasting of the anterior tibial and peroneal muscles
214
child comes with epilepsy with cafe au lait spots, angiofibromas over the nose and cheeks and a gew shagreen pathces.
what is this
tuberous sclerosis
215
mutation of TSC1 gene on chromosome 9 causes what
this produces hamartin
mutaztion of this causes tuberous scleorosis
216
what genes cause tuberous scleorisis
TSC1 gene- chromosome 9- hamartin
TSC2 gene- chromosome 16- tuberin
217
s and s of tuberous scleorisi
main feature is hamartomas = benign neoplastic growths of the tissue it orginates in
can affect: lungs, brain, heart, eyes, kidneys, skin
skin signs=
cafe au lait spots
angiofibromas across nose and cheeks
ash leaf spots
shagreen patches
poliosis - white hair patch in any hair
subungual fibromas
neuro=
epiplepsy
learning disability and developmental delay
othes:
rhabdomyomas in heart
gliomas
polycystick kidnneys
lymphangioleimyomatosis - often in lungs
retinal hamartomas
218
s and s of lymphangioleimyomatosis
oftens affects lungs
seen in tuberous sclerosis
lungs:
coguh, sob, haemoptysis, chest pai, pneumothroax
219
treat tuberous sclerosis
supportive
monitoring
treat compliations
220
what is the most common type of nneurofibrosmatosis
type 1
221
s and s of idiopathic intracranial ht
This is evidenced by the presence of diffuse headaches, blurred vision, pulsatile tinnitus (the 'woosh' sound she describes) and the bilateral papilloedema.
headache
blurred vision
papilloedema (usually present)
enlarged blind spot
sixth nerve palsy may be present
222
what class of antibiotics can increase risk of idiopathic intracranial haemorrhage
Lymecycline is in the tetracycline class of antibiotics - a class known to increase risk of developing this condition.
223
rf for idiopathic intracranial ht
young, overweight females.
Risk factors
obesity
female sex
pregnancy
drugs
combined oral contraceptive pill
steroids
tetracyclines
retinoids (isotretinoin, tretinoin) / vitamin A
lithium
224
management for idiopathic intracranial haemorrhage
weight loss
diuretics e.g. acetazolamide
topiramate is also used, and has the added benefit of causing weight loss in most patients
repeated lumbar puncture may be used as a temporary measure but is not suitable for longer-term management
surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure
225
what imaging would you use to look for demyelinating lesions eg. MS
MRI with contrast
226
whats wernickes dyspahsia
Wernicke's dysphasia: speech fluent, comprehension abnormal, repetition impaired
Important for meLess important
Wernicke’s dysphasia is correct. This results from damage to Wernicke’s area in the temporal lobe and impairs language comprehension, repetition of words and phrases. In Wernicke’s dysphasia speech is fluent with intact sentence structure, but is lacking meaning.
227
whats brocas dysphasua
dysphasia where the speech is non-fluent, unlike in this case, because Broca’s area in the frontal lobe connects with the motor cortex to produce the movements required to articulate the words. As a result, repetition of words is also poor. Comprehension is normal in patients with frontal lobe damage, as the language comprehension centres found in the temporal lobe, Wernicke’s area, are intact.
228
whats steven johnson syndrome and what drugs can casue the adverse affect
fevers
photophobia
rash
lamotrigine
NSAIDs
cephlasporins
sulphonomides
allopurinol
other anticonvulsants
229
whats webers syndrome
Weber's syndrome is a midbrain stroke syndrome that involves the fascicles of the oculomotor nerve resulting in
ipsilateral CN III palsy and contralateral hemiplegia or hemiparesis.
230
the empty delta sign is seen on venography
pt has bilateral papilloedema and headache
what is it
sagittal sinus thrombosis is associated with raised ICP and the 'empty delta sign' on venography.
231
lucid interval after injury- eg. awake 30 mins then collapse
biconvex on imaging of brain
what is this
acute extradural haermorrhage
its biconvex so not with the shape. ofthe head. like you throw a ball at someones head and its leaving a dent in it
cause often middle menigeal artery
232
acute subdural haemorrhage occurs due to what and what shape on imaing
due to shake of head
bridging veins
crescent shape- shape sape as the way the skull goes (cus its inside the mater so with the brain and skull)
Acute subdural haemorrhage occurs due to vein's rupture and results in the collection between brain and dura mater. These veins rupture due to sudden jolts or shake to the brain. It usually appears as crescent-shaped on CT scan.
233
what would wubarachnoid haemorrhage lead to
Sub-arachnoid haemorrhage would lead to stroke. The patient would usually present with sudden severe headache and vomiting.
234
whats cerebral contusion caused by and is
Cerebral contusion is a bruise of the brain tissue and usually occurs due to small blood vessel leaks into the brain tissue. It usually result in increase intracranial pressure. It usually occurs due to the brain coming to sudden stop against the inner surface of the skull. The typical causes include motor vehicle accidents or when the head strikes the ground.
235
what prophylaxis for cluster headaches
what use for acute attak
Verapamil is used for cluster headache prophylaxis. Sumatriptan is used as an acute rescue therapy (along with high-flow oxygen),
236
how does syringomyelia present
Syringomyelia classically presents with cape-like loss of pain and temperature sensation due to compression of the spinothalamic tract fibres decussating in the anterior white commissure of the spine
237
imporntant cisual field defects
Visual field defects:
left homonymous hemianopia means visual field defect to the left, i.e. lesion of right optic tract
homonymous quadrantanopias: PITS (Parietal-Inferior, Temporal-Superior)
incongruous defects = optic tract lesion;
congruous defects= optic radiation lesion or occipital cortex
238
Deficiency of what vitamin can cause Wernicke's encephalopathy and if left untreated can lead to irreversible Korsakoff's syndrome.
b1= thiamine
239
L3 nerve root compression
L3 nerve root compression
Sensory loss over anterior thigh
Weak hip flexion, knee extension and hip adduction
Reduced knee reflex
Positive femoral stretch test
240
L4 nerve root compression
Sensory loss anterior aspect of knee and medial malleolus
Weak knee extension and hip adduction
Reduced knee reflex
Positive femoral stretch test
241
L5 nerve root compression
Sensory loss dorsum of foot
Weakness in foot and big toe dorsiflexion
Reflexes intact
Positive sciatic nerve stretch test
242
S1 nerve root compression
Sensory loss posterolateral aspect of leg and lateral aspect of foot
Weakness in plantar flexion of foot
Reduced ankle reflex
Positive sciatic nerve stretch test
243
contralateral hemiparesis and sensory loss
lower extremity> upper extremity
which artery affected in stroke
anterior cerebral artery
244
contralateral hemiparesis and sensory loss
upper extremity> lower extremity
contralaterla homonymous hemianopia
aphasia
which artery affected in this stroke
middle cerebral artery
245
contralateral homonymous hemianopia with macula sparing
visual agnosia
which artery affected in this stroke
posteror cerebral artery
246
ipislateral CN3 palsy
contralateral weakness of upper and lower extrmitits
whats this and what affected
webers syndrome
branches of posterior cerebral artey that suply midbrain
247
ispilateral facial pain and temp loss
contrlateral limb/torso pain and temp loss
ataxia, nystagmus
posterior infeferior cerebellar artey
= lateral medullary syndrome/ wallenburg syndrome
248
ipislateral facial paralsyis and deafness
with also similar to posterios infeerior this is anterior infererior cerebellar artery = lateral pontine syndrome
249
amacurosis fugax= darkening of the vision in area casue
rentinal / opthamic artery stenosis
carotid artery stenosis
250
locked in syndrome casue
where they cant move/speak but can blink eyes and move eyes up and down
casue = basiliar artery affected
251
lacunar strokes present with what
either
isolated hemiparesis, hemisensory loss
or
hemoparesis with limb ataxia
strong association with ht
common sites: basal ganglia
thalamus
internal caspule
252
idiopathic intracranial ht treatment
acetazolamide- carbonic anhydrase inhibitor = reduce production of CSF
topiramate is another med to use in IIH
253
frontal lobe epilepsy
jackasonian march
clonic movements starting in one extremity and moving proximally through the body is typical of a Jacksonian March. This, combined with post-ictal weakness usually indicates a frontal lobe origin.
254
temporal lobe epilepsy
usually presents with automatisms, such as lip-smacking, grabbing, or plucking at clothes, along with sudden emotional disturbance or a feeling of deja vu
May occur with or without impairment of consciousness or awareness
An aura occurs in most patients
typically a rising epigastric sensation
also psychic or experiential phenomena, such as déjà vu, jamais vu
less commonly hallucinations (auditory/gustatory/olfactory)
Seizures typically last around one minute
automatisms (e.g. lip smacking/grabbing/plucking) are common
255
parietal lobe epilepsy
sensory disturbances, such as paraesthesia, electric shock type sensations, hallucinations, or dizziness
256
occipital epilepsy
typically visual, presenting with flashers and floaters, or lines in the vision
257
cerebellum indirectly cause epilepsy symptoms
the cerebellum can indirectly cause epileptic seizures, they are unlikely to originate in the cerebellum itself. Symptoms of cerebellar damage include gait disturbance, jerky movements, and speech disturbance
258
alzheimers dementia main feature
memory
259
vvascualr dementia main feature
mood
stepwise fashion of progression
ht major risk facotr
260
frontotemporal dementia main feature
earlier onset 45-65yrs
personaility, social, decsion,empathy= frontal lobe
speech, language and memory loss= temporal lobe
261
differntials for dementai
HIV related dementia
prion protien disease - CJD
depression!!
normal pressure hydrocephalus
mild cognitive impairment
262
confusion screen
calcium
FBC
U &E
LFT
CRP and ESR (urine test can be sent to labs if conufusion in elderly uti)
TFT- hypothryoidism
B12 and folate
glucose
263
blood test to differentiate between seixure and non-epileptic pseudo seizure
prolactin
true epileptic= raised prloactin
264
webers syndrome
Weber's syndrome is a form of midbrain stroke characterised by the an ipsilateral CN III palsy and contralateral hemiparesis
265
ipsilateral CN3 palsy and contralateral hemiparesis
webers syndrome
266
biceps reflex
C5,C6
267
internucelar opthamplegia
Internuclear ophthalmoplegia (INO) occurs due to a lesion of the medial longitudinal fasciculus (MLF), a tract that allows conjugate eye movement. This results in impairment of adduction of the ipsilateral eye. The contralateral eye abducts, however with nystagmus.
same eye cant adduct
other eye can abduct but nystagmus when it does
268
no matter waht the realpse is in what rx for MS relapse
oral methylprednisolone
269
foot drop
common peroneal nerve damage
270
analgesia headache managemnt
stop nsaids, triptans and paracetmaol immedisately
withdraw opiates sloewly (codeine)
271
contralteral homonymous hemianopia with macula sparing and visual agnosia
posterior cerebral artery
272
pituitary gland tumour eye changes
Bitemporal hemianopia, upper quadrant defect
273
stroke what side eye changess
same side as the parlasyis
the homonymous hemianopia is always on the same side as the paresis.
274
Primary open angle glaucoma in right eye
Unilateral peripheral visual field loss
275
bitemporal hemianopia
lesion of optic chiasm
upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma
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locked in syndrome - cant move or speak but can follow eye commands
which artery in this affected
basillar artery
blood vessel supplies the cerebellum, thalamus, occipital lobe, and brainstem. These strokes are rare and often devastating. There are 3 main presentations of patients experiencing a basilar artery infarct:
An acute decreased GCS and advanced motor symptoms.
Insidious, gradual deterioration in GCS and motor symptoms with a subsequent sudden advanced decrease in GCS and motor symptoms.
A 'herald hemiparesis' with associated headache and vision changes prior to the onset of permanent symptoms of motor loss
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Ipsilateral oculomotor palsy and contralateral weakness of the upper and lower extremity
branches of the posterior cerebral artery that supply the midbrain
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sensation of fine touch, proprioception and vibration are all conveyed in the
dorsal column
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brown sequard syndrome
tracts affeced:
1. Lateral corticospinal tract
2. Dorsal columns
3. Lateral spinothalamic tract
casues:
1. Ipsilateral spastic paresis below lesion
2. Ipsilateral loss of proprioception and vibration sensation
3. Contralateral loss of pain and temperature sensation
